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Section 7. Medical science
Section 7. Medical science
Abzalova Shakhnoza Rustamova, Cand.Sc., Department of Pathologic physiology, human anatomy,
histology, cytology and embryology, Tashkent Pediatric Medical Institute, senior lecturer E-mail: mbshakur@mail.ru Utekeeyeva Sanaubar Satullayevna, Nukus department of Tashkent Pediatric Medical Institute, Microbiology, medical biology and histology department, assistant
Kaldibayeva Akmaral Orinbasarovna, Tashkent Pediatric Medical Institute, Pharmacology and normal physiology department, assistant
Characteristic morphologic alterations in liver in experimental ischemic damage of brain
Abstract: Dysfunctions of liver in ischemic disorders are characterized by central dysfunctions of liver and often serve to be not only background together with which later severe hepatic diseases develop under influence of infections, intoxications and other impacts, but also act as an activator of deterioration of the general state. Keywords: cerebral ischemic insult, alterations in liver, morphology.
Topicality. It is known, that the main defecting factors, which are able to suppress the function ofliver, are, first of all, all the situations causing disorders of hepatic blood supply [1; 4; 6]. A damaged liver itself can change the progress of many states and organism's metabolisms as a whole, including pharmacologic impact of pharmaceutical agents [3; 2; 8]. Polypragmasia and a great amount of agents available in the modern staff of pharmacopoeia for ischemic insult, absence of a common standards for administration of agents and insignificant evidence of efficacy of the agents — all these complicates the functioning of liver and in complex negatively effects the status of patients with cerebral ischemic catastrophes.
Objective: is to study morphologic peculiarities of the liver status at the early terms of cerebral ischemic insult in experiment.
Materials and methods of the research. In experiment we performed incomplete ischemia of brain for creation of cerebral reperfusion injure mechanism. All the procedures of the experiment corresponded to the requirements of International rules of humane attitude to animals, stipulated in Sanitary rules of equipment and maintenance of experimental-biologic clinics (vivarium). The choice of the experiment object was conditioned by the resemblance of human and Wistar laboratory white rats' cerebral architectonics and similarity of the main hem dynamic parameters. The animals 250-280 grams in the age from 4 to 7 months were divided to 2 groups: 1st group included 8 rats, which had skin incision on neck above carotid artery on the left side and later sutur-
ing of the skin (pseudo operated); and the 2nd group included 9 rats with dissection of the left carotid artery, clipping for 20 minutes with further reperfusion and complete restoration of cerebral blood supply.
The follow-ups were performed in 1,3 and 7 days after ischemia-reperfusion. Verification of the ischemic insult was confirmed on the basis of the checking of photo optic preparations stained by Nissle's method. To obtain semi-thin cuts the temporal lobe tissue was fixed in 2.5% glutar aldehyde with further processing in compliance with the standard strategy in alcohols with growing concentration and filling in araldite. Semi-thin cuts were obtained with the help of ultra microtome LKB and stained by methylene blue and fuchsine.
Results and discussion. Macroscopically we noted: round anterior edge of liver, focal hyperemia and relevant thickening of the capsule, and smooth surface. In case of long-lasting process and severe ischemic cerebral lesion, mostly among old animals, liver becomes thick and "septal pattern" elements appear on its surface.
As a result of morphologic studies we detected appearance of small confocal areas of inflammatory reaction and dystrophic alterations, mostly in portal tracts, characterized by the elements of small focal periportal hepatitis. Singular rare small spotty inflammatory infiltrates can exceed portal stromae and go to peripheral parts of lobules without development of necrosis of hepatocytes, locating between hepatic cells — so-called discrete infiltrate; singular periportal necrosis develop rarely.
Characteristic morphologic alterations in liver in experimental ischemic damage of brain
Often at the early stages of experimental ischemic insult in rats we detect focal proliferation alterations inside lobules: clearly limited infiltrates of cells- derivatives of mononuclear phagocytes' system. Intensity of hem-tissue exchange significantly depends on the speed of blood flow in sinusoids, and it is, in its turn, associated with peculiarities of its structure.
Normally during the first day in periportal parts of hepatic lobule in experimental ischemic insult we can observe mostly straight and branched sinusoids. Later, to the 7th day periportal tracts up to the areas adjacent with the central vein are characterized by prevalence of branched sinusoids with clear tendency of anastomosis. And the significant characteristic feature was direct proportional link between the appearance of unulipodia and the degree of cerebral ischemia expression revealed by us.
Morphologic manifestations of ischemic cerebral catastrophes were disorders of beam structure of liver, intra lobular alternative manifestations with appearance of singular hepa-tocytes necrosis with accumulation of some macrophages, lymphocytes, neutrophils and foci of hepatocytes fatty dystrophy in these areas, proliferation and hypertrophy of stellate reticular endotheliocytes, edema and widening of portal tracts with infiltration by lymph histocyte elements and neutrophils, sometimes proliferation of periportal and intra lobular bile ducts and formation of lymphoid follicles.
In our research in experimental ischemic insult we noted a tendency for centralization of intra hepatic blood circulation linked with the presence of portal-portal anastomosis inside hepatic lobules and collaterals. Microscopically we detected polymorphism of hepatocytes (cells of various sizes, among which many bi and multinuclear ones, and with different sized nuclei), their swelling, resulting in the definition of beam structure. Protein (hydropic, balloon) and fatty dystrophy have small focal character, and it is difficult to define the expression of these alterations as characteristic or specific ones in a certain case. In various parts of hepatic lobules we can see small foci of parenchyma necrosis with destruction of argirofillic stromae and focal infiltrates of macrophages, lymphocytes, and neutrophils. There was explicit proliferation and hypertrophy of stellate reticular endotheliocytes (liver macrophages). Portal tracts were widened, edematous, with
moderate or weak infiltration with lymph histocyte elements with a mixture of neutrophils.
Thus, macroscopic alterations we observed, such as consolidation of liver with round anterior edge, focal hyperemia and some thickening of the capsule with smooth surface, appearance of "septal pattern" elements on its surface indicated high probability of further development of focal fibrosis.
Result of our research was confirmation of the opinion of many authority scientists, that in the acutest period of ischemic insult in liver there occurs narrowing of capillaries with slow down of the blood flow and aggregation of erythrocytes [5], and it plays a great part in the mechanism of hepatic blood supply disorder [7]. There was also narrowing of small veins, gradual widening of sinusoids with slow blood flow and aggregation of erythrocytes in them, and intra hepatic shunting of blood flow.
Presence of small confocal areas of inflammatory reaction with elements of dystrophic alterations mostly in portal tracts and periportal areas, i. e. in I zones. It is known? That exactly in these zones there is greater amount of oxygen and substances of metabolic reactions in comparison with others, while metabolic and regeneration activity of this zone is the most intensive; that's why we consider these areas to be first involving in the concomitant pathologic processes. Widening of portal tracts, its edema and infiltration with lymph histocyte structures testify the possibility of further development of sclerotic processes in these areas mostly moderate degree of expression. Clearly limited infiltrates of cells characterizing focal proliferative alterations inside lobules at the early stages of experimental ischemic insult in rats are manifestations of small spotty infiltrative granulomatous inflammatory process.
Conclusion. Dysfunctions of liver in ischemic disorders of central regulatory mechanisms are mostly variable, but not very explicit morphologically. According to some authors' opinion, often not only one, but several functions are disturbed, with morphologic confirmation revealed in our research. In our observations central dysfunctions of liver serve to be not only background together with which later severe hepatic diseases develop under influence of infections, intoxications and other impacts, but also act as an activator of deterioration of the general state.
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